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Human Immunodeficiency disorder (HIV) is a viral infection. The infection results from one of two similar retroviruses (HIV-1 and HIV-2) that destroy CD4+ lymphocytes and can impair cell-mediated immunity which increases the risk of certain infections and cancers (Cachay, 2019). When cell-mediated immunity is impaired, the immune system weakens and makes the body more susceptible to any type of infection that sees opportunity. HIV is spread through contact with infected body fluids such as saliva, blood, and semen. The pathophysiology includes the HIV cells to attach and penetrate host T cells via the CD4+ molecules and chemokine receptors. After the attachment process, HIV RNA and several HIV-encoded enzymes are released into the host cell (Cachay, 2019). This process results in multiple replications of the infected host cell. These mutations facilitate the generation of HIV which can resist control by the host’s immune systems and by antiretroviral drugs (Cachay, 2019). Compensatory mechanisms are present throughout the human body and evolution is a key factor in the impairment of several disease processes. RNAi is a novel target when directed at the viral TAR. When this has been tested, HIV can not mutate the target site. Instead several mutations indirectly compensated through upregulation. The RNAi represents a novel compensatory mechanism by which viruses can tune viral transcriptional regulation as an indirect mechanism to compensate for viral suppression (Leonard, J. N., et al, 2008). Depending on the infected host’s immune system, HIV can present as an acute febrile illness days to months after exposure to the virus. Determination of HIV is based on the CD4+ count. When the CD4+ count drops to <200/mcL nonspecific symptoms may worsen and succession of AIDS-defining illnesses will develop (Cachay, 2019). Behavior seems to be the largest risk factor in the pathophysiology and diagnosis of this disease process. Homosexual or bisexual men are at the highest risk of exposure to the infection. Anal-receptive intercourse poses the highest risk because mucous membrane inflammation facilitates HIV transmission (Cachay, 2019).
Systemic lupus erythematosus (SLE) is an autoimmune disease that results in multi-organ dysfunction. SLE is characterized by a loss of self-tolerance with activation of autoreactive T and B cells which then leads to production of pathogenic autoantibodies and tissue injury (Choi, Kim, & Craft, 2012). The kidneys are the primary targeted area that generates the initial dysfunction from this genetic pre-disposed disease. Even though genetics is a predisposition to the development of SLE, the cause remains unknown. The pathophysiology includes tissue injury through the release of inflammatory cytokines, as well as the aberrant activation of autoreactive T and B cells, which eventually leads to the pathogenic production of autoantibodies and then results in end-organ injury (Choi, Kim, & Croft, 2012). End-organ injury in SLE can present as acute renal failure, spleenomegaly, and enlarged lymph nodes. The cause of this presentation is based on an increased amount of circulating and activated basophils (Choi, Kim, & Craft, 2012). To regulate this autoimmune disease process, CD4+ cells are present. CD4+ T cells are critical players in the pathogenesis of SLE, they regulate B cell responses and also infiltrate target tissues, which eventually leads to tissue damage (Choi, Kim, & Craft, 2012).
There are similarities and differences between SLE and HIV. Each disease attacks the immune system which can cause an increased inflammatory response. However in SLE, the immune system is overactive, where as in HIV, the immune system is underactive (2019). Therefore, in SLE the body attacks healthy tissue and cells and in HIV, the body lacks an immune system to attack infections and the body becomes more susceptible to illness. Both immune disorders are due to the qualitative CD4+ T cell dysfunction that occurs prior to CD4 cell depletion. It is manifested by reduced responsiveness of CD4 cells to monocyte soluble antigens, which may include polyclonal B cell activation and reduced antibody response to specific immunogens (Fox & Isenburg, 2007).
References
Cachay, E. R. (2019). Human Immunodeficiency Virus (HIV) Infection – Infectious Diseases. Retrieved from https://www.merckmanuals.com/professional/infectious-diseases/human-immunodeficiency-virus-hiv/human-immunodeficiency-virus-hiv-infection
Choi, J., Kim, S. T., & Craft, J. (2012). Pathogensis of systemic lupus erythematosus update. Pathology, 44. doi: 10.1016/s0031-3025(16)32688-5. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3508331/
Fox, R. A>, & Isenberg, D. A. (2007). Human immunodeficiency virus infection in systemic lupus srythematosus. Arthritis & Rheumatism, 40(6), 1168-1172. doi: 10.1002/art.1780400623. Retrieved from https://onlinelibrary.wiley.com/doi/pdf/10.1002/art.1780400623
Leonard, J. N., Shah, P. S., Burnett, J., C., & Schaffer, D. V. (2008). HIV Ecades RNA Interference Directed at TAR by an Indirect Compensatory Mechanism. Cell Host & Microbe, 4(5), 484-494. n doi: 10.1016/j.chom.2008.09.008. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2742160/
What is lupus? (2019). Retrieved from https://www.lupus.org/resources/what-is-lupus
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